Yao H, Sadoshima S, Kuwabara Y, Ichiya Y, Fujishima M
Second Department of Internal Medicine, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Stroke. 1990 Dec;21(12):1694-9. doi: 10.1161/01.str.21.12.1694.
We performed clinical and neuroradiologic studies, including positron emission tomography, in five patients with vascular dementia of the Binswanger type. The clinical features of these cases consisted of slowly progressive dementia, together with vascular risk factors such as hypertension and often a history of minor stroke, and characteristic white matter lesions on brain computed tomograms or magnetic resonance images. Digital subtraction angiography of the cervical and intracranial arteries demonstrated no occlusive lesion in any patient. Both cerebral blood flow and the cerebral metabolic rate for oxygen were markedly reduced in the white matter (54-77% of control values), and both were decreased in the parietal (73% of control), frontal (74-80%), and temporal (74-83%) cortices, where no abnormalities were detected by brain computed tomography or magnetic resonance imaging. We conclude that vascular dementia of the Binswanger type may be caused by disconnection between the cerebral cortex and subcortical structures due to ischemic damage in the white matter.
我们对5例宾斯旺格型血管性痴呆患者进行了临床和神经放射学研究,包括正电子发射断层扫描。这些病例的临床特征包括缓慢进展的痴呆,伴有高血压等血管危险因素且常有轻度卒中病史,以及脑部计算机断层扫描或磁共振图像上的特征性白质病变。对颈内和颅内动脉进行的数字减影血管造影显示,所有患者均无闭塞性病变。白质中的脑血流量和脑氧代谢率均显著降低(为对照值的54% - 77%),顶叶(为对照值的73%)、额叶(74% - 80%)和颞叶(74% - 83%)皮质中的脑血流量和脑氧代谢率也均降低,而脑部计算机断层扫描或磁共振成像未在这些部位检测到异常。我们得出结论,宾斯旺格型血管性痴呆可能是由于白质缺血性损伤导致大脑皮质与皮质下结构之间的联系中断所致。